The present invention relates to a method to maintain isocapnia when breathing exceeds baseline breathing and a circuit therefor. Preferably, the circuit includes a non-rebreathing valve, a source of fresh gas, a fresh gas reservoir and a source of gas to be inhaled when minute ventilation exceeds fresh gas flow. Preferably the flow of the fresh gas is equal to minute ventilation minus anatomic dead space. Any additional inhaled gas exceeding fresh gas flow has a partial pressure of CO2 equal to the partial pressure of CO2 of arterial blood.
Venous blood returns to the heart from the muscles and organs partially depleted of oxygen (O2) and a full complement of carbon dioxide (CO2). Blood from various parts of the body is mixed in the heart (mixed venous blood) and pumped into the lungs via the pulmonary artery. In the lungs, the blood vessels break up into a net of small vessels surrounding tiny lung sacs (alveoli). The vessels surrounding the alveoli provide a large surface area for the exchange of gases by diffusion along their concentration gradients. After a breath of air is inhaled into the lungs, it dilutes the CO2 that remains in the alveoli at the end of exhalation. A concentration gradient is then established between the partial pressure of CO2 (PCO2) in the mixed venous blood (PvCO2) arriving at the alveoli and the alveolar PCO2. The CO2 diffuses into the alveoli from the mixed venous blood from the beginning of inspiration (at which time the concentration gradient for CO2 is established) until an equilibrium is reached between the PCO2 in blood from the pulmonary artery and the PCO2 in the alveolae at some time during breath. The blood then returns to the heart via the pulmonary veins and is pumped into the arterial system by the left ventricle of the heart. The PCO2 in the arterial blood, termed arterial PCO2 (PaCO2) is then the same as was in equilibrium with the alveoli. When the subject exhales, the end of his exhalation is considered to have come from the alveoli and thus reflects the equilibrium CO2 concentration between the capillaries and the alveoli. The PCO2 in this gas is the end-tidal PCO2 (PETCO2). The arterial blood also has a PCO2 equal to the PCO2 at equilibrium between the capillaries and alveoli.
With each exhaled breath some CO2 is eliminated and with each inhalation, fresh air containing no CO2 is inhaled and dilutes the residual equilibrated alveolar PCO2, establishing a new gradient for CO2 to diffuse out of the mixed venous blood into the alveoli. The rate of breathing, or ventilation (VE), usually expressed in L/min, is exactly that required to eliminate the CO2 brought to the lungs and establish an equilibrium PETCO2 and PaCO2 of approximately 40 mmHg (in normal humans). When one produces more CO2 (e.g. as a result of fever or exercise), more CO2 is carried to the lungs and one then has to breathe harder to wash out the extra CO2 from the alveoli, and thus maintain the same equilibrium PaCO2. But if the CO2 production stays normal, and one hyperventilates, then excess CO2 is washed out of the alveoli and the PaCO2 falls.
It is important to note that not all VE contributes to elimination of CO2. The explanation for this is with reference to the schematic in the lung depicted in FIG. 10. The lung contains two regions that do not participate in gas equilibration with the blood. The first comprises the set of conducting airways (trachea and bronchi) 100 that act as pipes directing the gas to gas exchanging areas. As these conducting airways do not participate in gas exchange they are termed anatomic dead space 102 and the portion of VE ventilating the anatomic dead space is termed anatomic dead space ventilation (VDan). The same volume of inhaled gas resides in the anatomic dead space on each breath. The first gas that is exhaled comes from the anatomic dead space and thus did not undergo gas exchange and therefore will have a gas composition similar to the inhaled gas. The second area where there is no equilibration with the blood comprises the set of alveoli 103 that have lost their blood supply; they are termed alveolar dead space 104. The portion of VE ventilating the alveolar dead space is termed alveolar dead space ventilation (VDalv). Gas is distributed to alveolar dead space in proportion to their number relative to that of normal alveoli (normal alveoli being those that have blood vessels and participate in gas exchange with blood). That portion of VE that goes to well perfused alveoli and participates in gas exchange is called the alveolar ventilation (VA). In FIG. 10, the numeral references 105 and 106 indicate the pulmonary capillary and the red blood cell, respectively.
Prior art circuits used to prevent decrease in PCO2 resulting from increased ventilation, by means of rebreathing of previously exhaled gas are described according to the location of the fresh gas inlet, reservoir and pressure relief valve with respect to the patient. They have been classified by Mapleson and are described in Dorsch and Dorsch pg 168.
Mapleson A
The circuit comprises a pressure relief valve nearest to the patient, a tubular reservoir and fresh inlet distal to the patient. In this circuit, on expiration, dead space gas is retained in the circuit, and after the reservoir becomes full, alveolar gas is lost through the relief valve. Dead space gas is therefore preferentially rebreathed. Dead space gas has a PCO2 much less than PaCO2. This is less effective in maintaining PCO2 than rebreathing alveolar gas, as occurs with the circuit of the present invention.
Mapleson B and C
The circuit includes a relief valve nearest the patient, and a reservoir with a fresh gas inlet at the near patient port. As with Mapleson A dead space gas is preferentially rebreathed when minute ventilation exceeds fresh gas flow. In addition, if minute ventilation is temporarily less than fresh gas flow, fresh gas is lost from the circuit due to the proximity of the fresh gas inlet to the relief valve. Under these conditions, when ventilation once again increases, there is no compensation for transient decrease in ventilation as the loss of fresh gas will prevent a compensatory decrease in PCO2.
Mapleson D and E
Mapleson D consists of a circuit where fresh gas flow enters near the patient port, and gas exits from a pressure relief valve separated from the patient port by a length of reservoir tubing. Mapleson E is similar except it has no pressure relief valve allowing the gas to simply exit from an opening in the reservoir tubing. In both circuits, fresh gas is lost without being first breathed. The volume of gas lost without being breathed at a given fresh flow is dependent on the pattern of breathing and the total minute ventilation. Thus the alveolar ventilation and the PCO2 level are also dependent on the pattern of breathing and minute ventilation. Fresh gas is lost because during expiration, fresh gas mixes with expired gas and escapes with it from the exit port of the circuit. With the present invention, all of the fresh gas is breathed by the subject.
There are many different possible configurations of fresh gas inlet, relief valve, reservoir bag and CO2 absorber (see Dorsch and Dorsch, pg. 205–207). In all configurations, a mixture of expired gases enters the reservoir bag, and therefore rebreathed gas consists of combined dead space gas and alveolar gas. This is less efficient in maintaining PCO2 constant than rebreathing alveolar gas preferentially as occurs with our circuit, especially at small increments of V above the fresh gas flow.